More than gut thinking needed in carnitine debate

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The next time someone says, “Our mind and our body are connected,” you should agree.

Nod your head in a professorial manner, touch your chin and ask, “Which one do you think is in charge?”

The human body is endowed with a three-pound brain and about three pounds of bacteria in your gut. Those microscopic critters aren’t listening to your brain. They respond like pond scum. Feed them the right thing and they procreate.

One kind of intestinal organism loves L-carnitine (“L” denotes the active form), an amino acid the body naturally produces to help create energy. It’s also ingested when we eat animal products, with the highest levels in red meats.

It’s worth learning about this stuff, but only if you want to understand how to give your brain an edge over your bacteria.

The carnitine arguments are hard to sort through, but the outcome promises to change your thinking about meat and heart disease. The economic impact has already heated the language of opponents.

Carnitine has been promoted as a dietary supplement. You may find it in pharmacies and elsewhere. You won’t find a label telling you what it does, certainly no warnings. It’s part of a dysfunctional regulatory system that incorporates the welfare of several industries in legislative fiat.

Let me summarize the current status of carnitine: It is a chemical that makes you either more or less likely to die of a heart attack in the next three years.

In April 2013, articles about carnitine appeared in two reputable medical journals. Within days, intestinal bacteria hit the fan. CBS News and the New York Times were among those who reported quickly and enthusiastically.

The American Meat Institute dug its heels into soft barnyard soil, with one author claiming meat was his daily vitamin (Beef Daily, April 11, 2013).

Serious researchers express interest in the findings and recognize the need to replicate the studies. That’s the next step before revising our position on important matters of health and science.

For readers of this column who aren’t health professionals, allow me to walk through the sequence of events that causes most cardiovascular events, especially heart attacks and strokes. I’ll follow by indicating where carnitine fits into the picture.

The term myocardial infarction, commonly called a heart attack, means that muscle (myo) in the heart (cardio) has been infarcted (cut off from its blood supply and dying). I was taught in medical school that cholesterol builds up in the lining of the arteries. The vascular wall thickens and eventually plugs off part or all of the blood flow. That idea fit with the fact that high cholesterol was associated with heart attacks and strokes.

It formed the basis for most of our therapeutic interventions, but it never explained why most victims don’t have high cholesterol levels. We’ve learned, and continue to learn, that other factors are at play.

Here’s an overview of the tragic road to a heart attack or a stroke:

Think of a loose wooden shingle on the side of a shed. It’s flapping in the wind. On close inspection, you discover there is a quarter-sized patch of wood-rot. It surrounds a rusty nail, and an ant colony has moved in. The analogy to a plaque in your artery works like this. More than one event contributed to the problem.

You are right to be concerned that involvement of one site means that there are more of them elsewhere. Blood flow, like the wind, pulsates and it destabilizes the point of narrowing. The spot that is ready to break open is called a vulnerable plaque.

If you study a vulnerable plaque, you’ll find that it’s made up of fatty materials, including cholesterol and there are white blood cells that are signs of inflammation. Inside the plaque, a microscope reveals areas of necrosis, dead cells, and minute hemorrhages.

The disaster is closing in now, but it began decades earlier. The end may follow a shouting match, a shovelful of heavy snow, or nothing you can point to. That’s when the plaque ruptures, releasing materials that attract platelets and set off the body’s clotting mechanism.

The clot may cause a diagnosable heart attack or stroke. Sometimes the blood will flow through a narrowed channel and the area will scar down, leaving a partial blockage. Over time these can damage the heart and result in heart failure.

Here’s the way carnitine seems to be involved.

The process of atherosclerosis, hardening or stiffening of the arteries begins early in life. Fatty materials adhere to the walls of our arteries. Cholesterol may come from burgers and fries, but our bodies make cholesterol on their own. Inflammatory cells invade the lining of the artery and carry fatty materials with them.

This part of the process appears to be dependent on a chemical TMAO. That’s where the gut bacteria are needed. Animal products, including eggs and seafood contain some carnitine, but the levels are highest in red meats. Certain bacteria thrive on carnitine.

When the breakdown product goes to the liver, that organ makes TMAO, which promotes plaque growth and, without the bacteria, you have very little TMAO and you have very little plaque development. That appears to be the truth, unless further studies find a hole in the logic.

I began by comparing intestinal bacteria to pond scum. In truth, some of our intestinal organisms promote good health. Don’t be too quick to decide you want to get rid of all of them. That nonsense has been the source of terrible misinformation and some deaths.

As usual, I’m running long and I want to explain how scientists have worked this out. Not everyone agrees with the conclusions, but most experts feel our way of looking at the leading cause of death in this country is changing.

Dr. Larry Mulkerin is a retired clinical professor and oncologist who lives in Walla Walla. A former U.S. Army Green Berets medical officer with experience in the Middle East, he also is the author of “The Ayatollah’s Suitcase,” a novel available at amazon.com and other online book retailers. He can be reached at mulkerin@charter.net.

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